Apurva Tadimari Prabhakar

This paper shows E2 activates the DNA damage response by displacing CIP2A from TOPBP1, promoting viral replication and cell proliferation through ATM activation and ATR inhibition.

This paper shows that HPV16 requires SMARCAL1 to recruit to viral and host replication forks, which is essential for its life cycle and prevents DNA damage and genome integration.

This study identifies novel host factors interacting with HPV16 E2 during differentiation using proximity proteomics, revealing a cooperative E2-TOPBP1-NCL axis critical for viral genome stability.

This paper develops a fibroblast co-culture model to predict drug responses in HPV+ cancers and shows it better predicts in vivo outcomes than in vitro alone.

This paper identifies a mitotic E2-TopBP1 complex that inactivates SIRT1, promoting E2 acetylation and stability through p300, which protects against ubiquitination and proteasomal degradation.

This study shows that HPV16 E2 protein interacts with TopBP1 to mediate plasmid segregation and stability during the viral life cycle, and that this interaction is essential for E2 expression and function.

This study shows that the E2-p53 interaction is critical for HPV16 life cycle, with disruption leading to anti-viral effects like reduced proliferation and increased DNA damage.

This paper shows that CK2 phosphorylation of HPV16 E2 on serine 23 promotes interaction with TopBP1, which is critical for plasmid retention and HPV16 immortalization of keratinocytes.

This study shows that HPV16 E6 and E7 proteins synergistically repress innate immune gene expression in the context of the full HPV16 genome, with neither protein alone sufficient for repression.